α2巨球蛋白受体识别形式与细胞受体结合后巨噬细胞中Akt/PDK信号的激活:沉默CREB基因的作用

IF 2.8 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

引用本文:张晓明,张晓明,“α - 2巨球蛋白受体与巨噬细胞中Akt/PDK信号的结合:抑制CREB基因的作用”,《细胞生物化学杂志》,第93期。5 (2004): 1020-1032, https://doi.org/10.1002/jcb.20233.The上述文章于2004年9月9日在线发表在Wiley在线图书馆(wileyonlinelibrary.com)上,经期刊主编Christian Behl;和Wiley期刊有限责任公司。由于第三方提出的担忧,已同意撤回。具体来说,在图2A和5A之间、图3和图3和图4B之间以及图4A和图6之间都发现了重复的图像元素。在所有情况下,这些图像元素被用来表示不同的实验条件。一项机构审查证实了这些担忧的有效性。因此,由于编辑对整个数据的准确性和完整性失去信任,并认为文章的结论无效,文章被撤回。作者已被告知撤稿的决定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RETRACTION: Activation of Akt/PDK Signaling in Macrophages Upon Binding of Receptor-Recognized Forms of α2-Macroglobulin to Its Cellular Receptor: Effect of Silencing the CREB Gene

RETRACTION: U. K. Misra, and S. V. Pizzo, “Activation of Akt/PDK Signaling in Macrophages Upon Binding of Receptor-Recognized Forms of α2-Macroglobulin to Its Cellular Receptor: Effect of Silencing the CREB Gene,” Journal of Cellular Biochemistry 93, no. 5 (2004): 1020–1032, https://doi.org/10.1002/jcb.20233.

The above article, published online on 9 September 2004 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 2A and 5A, within Figure 3 and between Figures 3 and 4B, and between Figures 4A and 6. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.

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来源期刊
Journal of cellular biochemistry
Journal of cellular biochemistry 生物-生化与分子生物学
CiteScore
9.90
自引率
0.00%
发文量
164
审稿时长
1 months
期刊介绍: The Journal of Cellular Biochemistry publishes descriptions of original research in which complex cellular, pathogenic, clinical, or animal model systems are studied by biochemical, molecular, genetic, epigenetic or quantitative ultrastructural approaches. Submission of papers reporting genomic, proteomic, bioinformatics and systems biology approaches to identify and characterize parameters of biological control in a cellular context are encouraged. The areas covered include, but are not restricted to, conditions, agents, regulatory networks, or differentiation states that influence structure, cell cycle & growth control, structure-function relationships.
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